Sleep apnea (SA) is a serious, potentially life-threatening condition that is far more common than generally understood. First described in 1965, SA is a breathing disorder generally characterized by brief interruptions of breathing during sleep. Generally speaking, there are two types of SA. Central sleep apnea, which is less common, occurs when the brain fails to send the appropriate signals to the breathing muscles to initiate respirations or, conversely, when the breathing muscles do not receive such signals. Obstructive sleep apnea is far more common and occurs when air is prevented from flowing into or out of a person's nose or mouth, although efforts to breathe continue. A third form of sleep apnea exists, mixed sleep apnea, and is exactly that—a mixture of the other two forms.
In a given night for a person having SA, the number of involuntary breathing pauses, or “apneic events,” may range from as low as one or two to as high as twenty or sixty per hour. These breathing pauses are almost always accompanied by snoring, although not everyone who snores is sleep apnetic. SA can also be characterized by choking sensations. In any event, the frequent interruptions of deep, restorative sleep often leads to excessive daytime sleepiness and may be associated with an early morning headache. Moreover, SA may be associated with irregular heartbeat, high blood pressure, heart attack and stroke.
SA occurs in all age groups and within both sexes; however, it is more common in men (although that may be because SA is underdiagnosed in women) and possibly young persons of African descent. Within the United States, it has been estimated that as many as 18 million Americans have SA. Four percent of middle-aged men and two percent of middle-aged women have SA, along with excessive daytime sleepiness. People most likely to have or develop SA include those who snore loudly and also who are overweight, and those who have high blood pressure or have some physical abnormality in the nose, throat or other parts of the upper respiratory airways. Additionally, SA seems to run in some families, suggesting a possible genetic basis.
Certain mechanical and structural anomalies in the respiratory airways of a sleep apnetic person cause the interruptions in breathing during sleep. In some people, SA onset occurs when the throat muscles and tongue relax during sleep and partially block the opening of the respiratory airways. When the muscles of the soft palate at the base of the tongue and the uvula relax and sag, the respiratory airway becomes blocked, making breathing labored and noisy or even stopping altogether. SA also can occur in obese people when an excess amount of tissue in the respiratory airways causes them to be narrowed. With a narrowed respiratory airway, the person continues efforts to breathe, but air cannot easily flow into or out of the nose or mouth. Unknown to the person, this results in heavy snoring, periods of no breathing and frequent arousals (causing abrupt changes from deep sleep to light sleep). Ingestion of alcohol and sleeping pills increases the frequency and duration of breathing pauses in people with SA.
During the apneic event, the person is unable to breathe in oxygen and to exhale carbon dioxide, resulting in low levels of oxygen and increased levels of carbon dioxide in the blood. The reduction in oxygen and increase in carbon dioxide alert the brain to attempt to resume breathing by causing what is termed an “arousal.” With each arousal, a signal is sent from the brain to the upper respiratory airway muscles to open the airway; breathing is eventually resumed, often with a loud snort or gasp. Frequent arousals, although necessary for breathing to restart, prevent the patient from getting enough restorative deep sleep.
As a result of the serious disturbances in their normal sleep patterns, people with SA often feel extremely sleepy during the day and, as such, their concentration and daytime performance suffer. The consequences of SA range from annoying to life-threatening. They include symptoms of depression, irritability, sexual dysfunction and learning and memory difficulties, as well as falling asleep while at work, on the phone or driving. Untreated SA patients are at least three times as likely to encounter a dangerous condition or an accident as a result of SA, such as, for example, automobile or other machinery accidents. Moreover, it has been estimated that up to fifty percent of SA patients have high blood pressure. Finally, it has recently been shown that the risk for heart attack and stroke may also be increased in those with SA.
The specific therapy for SA is tailored to the individual patient based on medical history, physical examination and the results of any polysomnographic tests done on the patient. Medications are generally not effective in the treatment of SA.
Nasal continuous positive airway pressure (CPAP) is the most common effective treatment for SA. In this procedure, the patient wears a mask (sometimes referred to as a CPAP sleeve or device) over the head during sleep, and pressure from an air blower forces air through the nasal passages. The air pressure is variably adjusted so that it is just enough to prevent the throat from collapsing during sleep. The pressure is continuous and constant.
Variations of CPAP devices attempt to minimize side effects that sometimes occur, such as nasal irritation and drying, facial skin irritation, abdominal bloating, mask leaks, sore eyes and headaches. Some versions of CPAP devices vary the pressure to coincide with the person's breathing pattern, and other CPAP devices start with low pressure, slowly increasing it to allow the person to fall asleep before the full prescribed pressure is applied.
An example of such a mask is illustrated in FIG. 1. As shown in FIG. 1, mask 10 comprises top strap 12 and bottom strap 14. Top strap 12 and bottom strap 14 securely and snugly hold nosepiece 16 to the face of wearer 18. Pressurized air is forced from an air blower (not shown) through breathing tube 20 into the nasal respiratory airway of wearer 18 in an attempt to keep the nasal respiratory airway open. While the prior art disclosed in FIG. 1 attains the goal of forcing air through the nasal respiratory airway, it does not inhibit the use of the mouth for breathing.
To inhibit such a use of the mouth, sleep apnetics have come to wear chinstraps, such as that illustrated by FIG. 2. In FIG. 2, chinstrap 22 is illustrated as comprising chin portion 24 and adjustable strap portion 26. Wearer 18, when using chinstrap 22, adjusts adjustable strap portion 26 to provide a snug fit of chin portion 22 on the chin of wearer 18. This maintains a closed mouth during sleep, forcing wearer 18 to breathe only through the nose. Additionally, chin portion 22 defines chin portion opening 28. Another example of such a chinstrap device is disclosed in U.S. Pat. No. 5,361,416, issued to Petrie et al. However, like the mask illustrated in FIG. 1, the chinstrap illustrated in FIG. 2 and in Petrie only address one aspect of SA; that being the inhibition of the use of the mouth during sleep. See, e.g., Petrie, Abstract.
Thus, although such devices attempting to cure SA do exist, the devices in existence suffer from a number of disadvantages. Most noticeable is the fact that neither device can completely assist the wearer in treating SA or any other oxygen-deprivation disorders. For instance, wearing the mask illustrated in FIG. 1 does not force the mouth of the wearer closed during sleep. Likewise, wearing the chinstrap illustrated in FIG. 2 does not ensure the nasal respiratory airways will remain open during sleep. Instead, some sleep apnetics have had to resort to wearing combinations of both the mask and the chinstrap.
However, even the simultaneous use of the mask and the chinstrap, as presently known, has its disadvantages. First and foremost, effectiveness is a major issue. Experiments have shown that one or both of the devices tends to slip off the wearer's head during sleep, causing the same ineffective situation as if the wearer had been wearing only one of the devices. Secondly, the presence of extra straps on the face leads to an improper fit of the nosepiece to the wearer's nose. Comfort is an additional factor—the use of both devices simultaneously has caused, in experiments, chafing and other friction-based indications on the wearer's face.
Thus, the need exists for an improved headgear apparatus for effectively treating the symptoms of SA (and other oxygen deprivation disorders), while at the same time overcoming the above-stated disadvantages.